8 results match your criteria: "The Lankenau Hospital and Medical Research Center[Affiliation]"

Study Objectives: To determine the frequency of classical markers of non-rapid eye movement (NREM) parasomnias--hypersynchronous delta sleep (HSD) electroencephalogram waves and sudden arousals from slow-wave sleep (SWS)--in patients without histories of somnambulism or other NREM parasomnias.

Design: Retrospective review.

Setting: Sleep disorders center laboratory.

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Background: Patients with inducible sustained ventricular tachycardia (VT) sometimes receive intravenous procainamide during electrophysiologic testing. Unfortunately, the responses to intravenous and subsequent oral drug therapy are variable and may be discordant.

Hypothesis: It was the aim of this study to determine whether this variability might be explained by heterogeneity in the electropharmacologic response, even in a homogeneous population.

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beta-Adrenergic stimulation of cardiac L-type Ca(2+) channels is severely impaired in hypertrophied and failing hearts of both experimental animals and humans. The aim of this study was to test the hypothesis that chronic treatment of renovascular hypertension with captopril restores normal beta-adrenergic responsiveness of L-type Ca(2+) channels in cardiac myocytes. Left ventricular hypertrophy was induced in rabbits by unilateral renal artery banding and contralateral nephrectomy.

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In freshly-isolated, single, smooth muscle cells of rabbit coronary arteries, an inward rectifier K+ current [IK(IR)] was identified using the whole-cell voltage-clamp technique. The current/voltage (I/V) relationship of IK(IR) showed strong inward rectification with a very small outward current when the smooth muscle cells were dialyzed with a pipette solution containing Mg2+. However, dialyzing the cells with a nominally Mg2+-free pipette solution revealed a significant outward current hump in the I/V relation of IK(IR), suggesting that the strong inward rectification of IK(IR) is partly due to the inhibitory effects of internal Mg2+.

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Recent studies indicate that regression of left ventricular hypertrophy (LVH) normalizes the in situ electrophysiological abnormalities of the left ventricle. This study was designed to determine whether regression of LVH also normalizes the abnormalities of individual membrane currents. LVH was induced in rabbits by renal artery banding.

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A diagnosis of severe obstructive sleep apnea was made after a 52-year-old hypertensive man developed a large intracranial hemorrhage. Therapeutic noninvasive positive pressure ventilation (NPPV) for obstructive sleep apnea and hypoventilation was complicated by transient unilateral orbital herniation. As best as can be determined, this represents a new, potentially deleterious side effect of NPPV.

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Atrial fibrillation (AF) is a common arrhythmia in patients with hypertensive heart disease. In addition, the presence of hypertension in patients with AF constitutes an important risk factor for the development of thromboembolic events and probably also selects out those individuals who may be resistant to drug therapy. AF in patients with hypertensive heart disease may lead to a number of serious clinical sequelae including stroke, left atrial myopathy, left ventricular dysfunction, and congestive heart failure.

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Background: Left ventricular hypertrophy (LVH) is associated with multiple cellular electrophysiological abnormalities, susceptibility to ventricular arrhythmias, and an increased risk of sudden death. Several pharmacological therapies have been shown to produce regression of hypertrophy, but the value of regression is unclear. The present study examines whether pharmacological regression of LVH has effects on the susceptibility to ventricular arrhythmia or the cellular electrophysiological abnormalities of LVH.

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